欢迎访问《茶叶科学》,今天是

六堡茶对胰岛素抵抗3T3-L1脂肪细胞糖脂代谢的影响

  • 滕翠琴 ,
  • 刘仲华 ,
  • 龚受基 ,
  • 彭雨轩 ,
  • 马蕊
展开
  • 1. 国家植物功能成分利用工程技术研究中心,湖南 长沙 410128;
    2. 湖南农业大学茶学教育部重点实验室,湖南 长沙 410128;
    3. 桂林医学院药学院,广西 桂林 541004;
    4. 湖南城市学院黑茶研究所,湖南 益阳 413000;
    5. 广西职业技术学院,广西 南宁 530226
滕翠琴(1986— ),女,广西南宁人,硕士研究生,主要从事功能成分开发与利用研究。

收稿日期: 2013-07-12

  修回日期: 2013-09-16

  网络出版日期: 2019-09-03

基金资助

国家茶叶产业技术体系研究项目(CARS-23-10B)、国家自然科学基金项目(31100502)资助

Effect of Liupao Tea on Glucose and Lipid Metabolism in Palmitate-induced Insulin Resistance 3T3-L1 Adipocytes

  • TENG Cuiqin ,
  • LIU Zhonghua ,
  • GONG Shouji ,
  • PENG Yuxuan ,
  • Ma Rui
Expand
  • 1. National Research Center of Engineering & Technology for Utilization of Botanical Functional Ingredients, Changsha 410128, China;
    2. Key Lab of Tea Science, Ministry of Education, Hunan Agricultural University, Changsha 410128, China;
    3. College of Pharmacy, Guilin Medical University, Guilin 541004, China;
    4. Dark Tea Studies Insitute, Hunan City University, Yiyang 413000, China;
    5. Guangxi Vocational & Technical College, Nanning 530226, China

Received date: 2013-07-12

  Revised date: 2013-09-16

  Online published: 2019-09-03

摘要

采用软脂酸诱导3T3-L1脂肪细胞胰岛素抵抗后,给予不同剂量的六堡茶水提物治疗,探讨六堡茶对胰岛素抵抗3T3-L1脂肪细胞的糖脂代谢的影响。结果表明,1 mmol·L-1的软脂酸对3T3-L1脂肪细胞作用24 h后,葡萄糖摄取量减少,建立胰岛素抵抗模型。六堡茶对模型细胞干预24 h后,与模型组比较,细胞培养基的残留液中葡萄糖和游离脂肪酸的含量降低;对糖脂代谢相关关键酶(己糖激酶、6-磷酸果糖激酶-1、丙酮酸激酶、甘油-3-磷酸酰基转移酶)和葡萄糖转运子基因表达都有上调作用,并下调乙酰辅酶A羧化酶、蛋白酪氨酸磷酸酯酶1B基因表达。低剂量的六堡茶下调肉碱脂酰转移酶-I基因的表达,但是高剂量能显著上调肉碱脂酰转移酶-I基因表达。实验证明了六堡茶能够提高胰岛素抵抗3T3-L1脂肪细胞对葡萄糖的摄取能力,同时促进细胞内糖脂代谢,六堡茶有改善3T3-L1脂肪细胞胰岛素抵抗的作用。

本文引用格式

滕翠琴 , 刘仲华 , 龚受基 , 彭雨轩 , 马蕊 . 六堡茶对胰岛素抵抗3T3-L1脂肪细胞糖脂代谢的影响[J]. 茶叶科学, 2014 , 34(3) : 230 -238 . DOI: 10.13305/j.cnki.jts.2014.03.004

Abstract

To investigate the effect of Liupao tea on glucose and lipid metabolism in palmitate-induced insulin resistance 3T3-L1 adipocytes. Glucose intake decreased and insulin resistance was induced in 3T3-L1 adipocytes after incubation in 1mmol/L palmitate for 24 hours. Compared with the model group, the concentrations of glucose and NEFA decreased along with the increase of Liupao tea concentrations in medium. The mRNA expression of key enzyme for glycolysis of glucose (Hexokinase, 6-phosphofructokinase-1, and pyruvatekinase) and the Lipid-Metabolism-Related Enzymes (Sn-glycerol-3-phosphate acyltransferase) significantly increased in the Liupao tea groups comparing with model sample. Meanwhile the glucose transporter 4 mRNA expression was also increased and the acetyl-CoA carboxylase, protein tyrosine phosphatase 1B mRNA expression was decreased. Low doses of Liupao tea reduced carnitine palmitoyl transferase I mRNA expression while high doses significantly raised it. Research proved that Liupao tea were able to increase glucose uptake and activate the glucolipid metabolic pathways. Liupao tea showed the effect of improving insulin resistance induced by palmitate in 3T3 -L1 adipocytes.

参考文献

[1] WU Y, DING L, XIA H, et al. Analysis of the major chemical compositions in Fuzhuan brick-tea and its effect on activities of pancreatic enzymes in vitro[J]. African Journal of Biotechnology, 2010, 9(40): 6748-6754.
[2] 傅冬和, 刘仲华, 黄建安, 等. 茯砖茶加工过程中主要化学成分的变化[J]. 食品科学, 2008, 29(2): 64-67.
[3] ZHANG L, ZHANG Z-Z, ZHOU Y-B, et al. Chinese dark teas: Postfermentation, chemistry and biological activities[J]. Food Research International, 2013, 53(2): 600-607.
[4] LU C-H, HWANG L S.Polyphenol contents of Pu-Erh teas and their abilities to inhibit cholesterol biosynthesis in Hep G2 cell line[J]. Food Chemistry, 2008, 111(1): 67-71.
[5] FU D, RYAN E P, HUANG J, et al. Fermented Camellia sinensis,Fu Zhuan Tea, regulates hyperlipidemia and transcription factors involved in lipid catabolism[J]. Food Research International, 2011, 44(9): 2999-3005.
[6] 龚受基. 六堡茶和茉莉花改善胰岛素抵抗功效及机制研究[D]. 长沙: 湖南农业大学, 2012: 49-79.
[7] 彭静静. 六堡茶的降血脂功能性研究[D]. 南宁: 广西大学, 2012: 28-38.
[8] SKRZYPSKI M, KACZMAREK P, LE T, et al. Effects of orexin A on proliferation, survival, apoptosis and differentiation of 3T3-L1 preadipocytes into mature adipocytes[J]. FEBS Lett, 2012,586(23):4157-4164.
[9] CHANGSUK K, JUNGAE K, SEKWON K.Anti-obesity effect of sulfated glucosamine by AMPK signal pathway in 3T3-L1 adipocytes[J]. Food Chem Toxicol, 2009, 47(10): 2401-2406.
[10] GAO C-L, ZHU C, ZHAO Y-P, et al. Mitochondrial dysfunction is induced by high levels of glucose and free fatty acids in 3T3-L1 adipocytes[J]. Mol Cell Endocrinol, 2010, 320(1/2): 25-33.
[11] KERSHAW E E, FLIER J S.Adipose tissue as an endocrine organ[J]. J Clin Endocrinol Metab, 2004, 89(6): 2548-2556.
[12] CAPURSO C, CAPURSO A.From excess adiposity to insulin resistance: The role of free fatty acids[J]. Vascul Pharmacol, 2012, 57(2/4): 91-97.
[13] SUKHATME V P, CHAN B.Glycolytic cancer cells lacking 6-phosphogluconate dehydrogenase metabolize glucose to induce senescence[J]. FEBS Lett, 2012, 586(16): 2389-2395.
[14] PAPAGIANNI M, AVRAMIDIS N.Lactococcus lactis as a cell factory: A twofold increase in phosphofructokinase activity results in a proportional increase in specific rates of glucose uptake and lactate formation[J]. Enzyme Microb Technol, 2011, 49(2): 197-202.
[15] GUO X, LI H, XU H, et al. Glycolysis in the control of blood glucose homeostasis[J]. Acta Pharmaceutica Sinica B, 2012, 2(4): 358-367.
[16] CARPENTIER A C.Postprandial fatty acid metabolism in the development of lipotoxicity and type 2 diabetes[J]. Diabetes Metab, 2008, 34(2): 97-107.
[17] KOK B, BRINDLEY D N.Myocardial Fatty Acid metabolism and lipotoxicity in the setting of insulin resistance[J]. Heart Fail Clin, 2012, 8(4): 643-661.
[18] TUEI V C, HA J-S, HA C-E.Effects of human serum albumin complexed with free fatty acids on cell viability and insulin secretion in the hamster pancreatic -cell line HIT-T15[J]. Life Sci, 2011, 88(17): 810-818.
[19] FOSTER D W.The role of the carnitine system in human metabolism[J]. Ann N Y Acad Sci, 2004, 1033(1): 1-16.
[20] CHIU T T, JENSEN T E, SYLOW L, et al. Rac1 signalling towards GLUT4/glucose uptake in skeletal muscle[J]. Cell Signal, 2011, 23(10): 1546-1554.
[21] BERENGUER M, MARCHAND-BRUSTEL Y L, GOVERS R. GLUT4 molecules are recruited at random for insertion within the plasma membrane upon insulin stimulation[J]. FEBS Lett, 2010, 584(3): 537-542.
[22] WANG N, ZHANG D, MAO X, et al. Astragalus polysaccharides decreased the expression of PTP1B through relieving ER stress induced activation of ATF6 in a rat model of type 2 diabetes[J]. Mol Cell Endocrinol, 2009, 307(1): 89-98.
[23] 张栩颜, 黄宇声, 刘冠萍, 等. 六堡茶对高脂血症小鼠血脂及脂质过氧化的影响[J]. 医学理论与实践, 2013, 26(5): 563-564.
文章导航

/